Keratopathy is a group of heterogeneous diseases of the cornea that lead to the development of a similar clinical picture. Regardless of the form, the common manifestations of pathology are hyperemia, a feeling of a foreign body or sand in the eyes, photophobia, pain syndrome. To establish a diagnosis, it is necessary to collect anamnestic data, conduct an external examination and biomicroscopy using a slit lamp. Treatment includes etiotropic (depending on the form of the disease) and pathogenetic therapy (moistening of the cornea with artificial tear preparations, applying a pressure bandage).
Keratopathy is a group of diseases of acquired or congenital genesis, which are accompanied by a violation of the integrity of the surface layers of the cornea. Aphakic, pseudoaphakic, cordaronic and neurotrophic keratopathies most often develop in old age, due to organic changes in the organ of vision. The lipoid lesion of the epithelial cells of the cornea is hereditary and manifests itself in the puberty period. Other forms of keratopathy in ophthalmology are equally common among all age categories. The male sex is more predisposed to the development of this pathology. In the case of congenital forms, the conductors of the disease are women.
There is a clear connection between the etiology of keratopathy and its clinical form. The most common cause of the threadlike form of the disease is dry eye syndrome, often combined with autoimmune pathology (Sjogren’s syndrome). Keratoconjunctivitis, recurrent corneal erosion, the imposition of mono- or binocular dressing in the postoperative period can also act as provoking factors. In rare cases, the pathology develops against the background of a neurotrophic or chronic bullous form. Exposure keratopathy occurs due to drying out of the constantly open cornea. This condition is observed with facial nerve paralysis, ectropion, nocturnal lagophthalmos or after blepharoplasty.
Herpes simplex virus, stroke, complications after surgery on the trigeminal nerve, benign or malignant neoplasms lead to a violation of the innervation and trophism of the cornea. In turn, the effect of high temperatures or ultraviolet radiation is a trigger for the development of thermal or ultraviolet keratopathy. The most common causes of the ribbon–shaped form are chronic uveitis, interstitial inflammation of the cornea, glaucoma. Less often, pathology occurs against the background of hypercalcemia, gout or chronic mercury intoxication.
Aphakic or pseudoaphakic bullous keratopathy is the result of a combination of factors such as endothelial damage (primary Fuchs dystrophy), intraocular edema, friction of the vitreous body or artificial lens on the cornea. As a rule, the disease develops after phacoemulsification, implantation of an artificial optical lens or surgery for glaucoma. The lipoid form is more often of hereditary origin or is associated with an acquired violation of lipid metabolism. Drug-induced pathology is only corneal damage due to prolonged use of Cordarone. The etiology of the development of Tygeson’s superficial point keratopathy has not been established.
From a clinical point of view, there are threadlike, exposure, neurotrophic, ribbon-like, aphakic, pseudoaphakic, cordaronic, lipoid, thermal, ultraviolet forms and surface point keratopathy of Tigeson. Common symptoms for all variants are hyperemia of the eyes, foreign body sensation, photophobia and pain in the eyes of varying intensity. A specific sign is corneal opacity, which patients identify independently. The degree of visual acuity reduction depends on the severity of the eyesore and edema. Swelling of the cornea often develops after injury.
Exposure keratopathy is characterized by an increase in clinical manifestations in the morning and their decrease during the day. With neurotrophic origin, edema of the eyelids and loss of corneal sensitivity are added to the main symptoms. The clinic of damage to the cornea when exposed to high temperature or ultraviolet radiation is similar. Classic manifestations are complemented by lacrimation, decreased visual acuity, the appearance of “fog” or “shroud” in front of the eyes. An early sign of the disease is a feeling of pain or burning of the eyes. The severity of symptoms increases 6-12 hours after the action of the etiological factor.
Tigeson’s superficial point keratopathy is a bilateral eye lesion characterized by a chronic course with stages of exacerbations and remissions. Visual acuity decreases slightly. A feature of the aphakic bullous form is the swelling of the cornea in the area of lens removal. As a rule, pathology develops after surgery for cataracts. An asymptomatic course is observed only with ribbon-like keratopathy. The severity of clinical manifestations of the cordarone form depends on the duration of administration and dosage of the drug. The use of Cordarone or Amiodarone for 6 months at a standard dose provokes the development of keratopathy in an average of 85% of patients.
The main methods of diagnosis of keratopathy are external eye examination and biomicroscopy using a slit lamp. Additionally, visometry, ophthalmoscopy and tonometry are performed. External examination with filamentous keratopathy allows you to identify short formations consisting of epithelial cells and mucus. These structures resemble threads that are attached to the anterior surface of the cornea. For better visualization, fluorescein staining is used, since filamentous elements are able to accumulate this dye. With the help of biomicroscopy, conjunctival injection and superficial spot keratitis can be detected. The latter is also determined by thermal or ultraviolet damage to the cornea.
In case of exposure keratopathy, it is necessary to evaluate the function of eye closure. In most patients, deformity of the eyelids or pathology of the facial nerve is detected. Biomicroscopy allows us to confirm secondary keratitis in the lower parts of the cornea. With neurotrophic lesions of the cornea, epithelial defects are well stained with fluorescein. Ulcerative defects are more often oval in shape with gray elevated edges. If it is not possible to establish the etiology of the disease, it is necessary to conduct an MRI of the brain for a stroke or tumor formation. With Tigeson keratopathy, the results of biomicroscopy are ambiguous. In the central parts, gray-white corneal opacities are found, which often have an irregular shape, elevated edges and are not stained with synthetic dyes.
The ribbon-like form of the disease is characterized by the formation of calcinates in the form of plaques of a porous structure in the zone of the palpebral slit at the level of the anterior boundary membrane. To establish the etiology, it is necessary to determine the level of calcium and uric acid in the blood. In bullous keratopathy, the condition of the cornea should be assessed for defects in the surface layer. By the method of angiography with fluorescein, cystic edema of the macula can be detected. With the help of tonometry, it is necessary to determine the degree of increase in intraocular pressure. Lipoid and cordarone keratopathy are accompanied by the appearance of pathological inclusions in epithelial cells, which is caused by the accumulation of metabolic products of the drug or lipid metabolism. Their presence can be confirmed by electron microscopy. All patients need to determine visual acuity by visiometry and assess the condition of the fundus by ophthalmoscopy.
In all forms of keratopathy, therapeutic measures should begin with etiotropic therapy of the underlying disease. Pathogenetic treatment is reduced to moisturizing the cornea (in the absence of defects) with artificial tear preparations and moisturizing ointments. With filamentous keratopathy, removal of pathological formations under regional anesthesia is indicated. With a ribbon-like shape, it is necessary to remove the plaque with the subsequent use of antibiotics. Damage to the cornea due to drying requires the application of a special bandage that will keep the eyelids closed until the elimination of the underlying disease (ectropion, lagophthalmos).
The tactics of treatment of neurotrophic keratopathy depends on the results of biomicroscopy. When spot injuries are detected, the use of artificial tear preparations is recommended. A small defect can be eliminated by topical application of erythromycin ointment and a pressure bandage for 24 hours. Next, the ointment is used 3-4 times a day for 4 days. If an infected corneal ulcer is detected, antibacterial therapy should be prescribed against the background of mydriatics. Treatment of corneal injuries of thermal or ultraviolet origin includes the local use of M-cholinoblockers, sympathomimetics and antibacterial ointment, as well as bandages for 24 hours. With severe pain syndrome, oral administration of analgesics is indicated.
The moderate and severe form of Tigeson’s keratopathy is an indication for the appointment of topical glucocorticosteroids or the use of therapeutic contact lenses. In case of bullous corneal lesion, sodium chloride drops are recommended for relieving edema and anti-glaucoma drugs with increased intraocular pressure. Progressive decrease in visual acuity requires corneal transplantation.
Prognosis and prevention
Specific measures for the prevention of keratopathy have not been developed. Patients are advised to monitor eye hygiene. With prolonged visual load, special means should be used to moisturize the cornea, do gymnastics and short breaks. Patients with a genetic predisposition or when taking Cordarone for 6 months need to be examined by an ophthalmologist 2 times a year.
With timely treatment, the prognosis for keratopathy is favorable for life and work capacity. The progression of pathology can be the cause of complete loss of vision, which leads to disability of the patient.